Increased sympathoexcitatory reflex induced by myocardial ischemic nociceptive signaling via P2X2/3 receptor in rat superior cervical ganglia.

The restructuring of cardiac innervation after myocardial ischemic injury, which is often associated with an increased sympathoexcitatory reflex characterized by an increase in blood pressure and sympathetic nerve activity. This study observed whether P2X(2/3) receptor in rat superior cervical ganglion (SCG) played a role in the increased sympathoexcitatory reflex induced by myocardial ischemic nociceptive signaling. The findings showed that the systolic blood pressure, heart rate and respiration in the myocardial ischemic rats were higher than those in control rats. The content of adenosine 5'-triphosphate (ATP) from myocardial ischemic group was higher than that from control group. After myocardial ischemic rats were treated with selective P2X(2/3) receptor antagonist A-317491, the content of ATP in SCG was reduced. Coexpression value of P2X(2), P2X(3) and tyrosine hydroxylase (TH) in the SCG and myocardial tissues of myocardial ischemic group was increased significantly, compared with that in the SCG and myocardial tissues of control group. The expression value of P2X(2), P2X(3) and TH in the SCG and myocardial tissues of myocardial ischemic rats treated with A-317491 was decreased. The amplitude of the currents was much larger in myocardial ischemic group than that obtained in control group after administration of ATP with the same concentration. After the myocardial ischemic rats were treated with A-317491, ATP-activated currents were reduced. The myocardial ischemic injury induced an increase in the expression of P2X(2/3) receptor colocalization with TH and a hypersensitivity state of SCG neurons to ATP, which led to the increased sympathoexcitatory reflex. 2010 Elsevier Ltd. All rights reserved.